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目的镉(Cd)诱导猪肾近曲小管上皮细胞(LLC-PK1)凋亡及其对胞内蛋白激酶B(PI3K/Akt)和胞外信号调节激酶(ERK1/2)表达的影响。方法应用不同浓度Cd(0、10、20、40、50μmol/L)作用LLC-PK112 h和40μmol/L Cd作用LLC-PK1不同时间(0、3、6、12、24 h),采用蛋白免疫印迹法检测细胞内蛋白激酶B(PI3K/Akt)和胞外信号调节激酶(ERK1/2)及其磷酸化蛋白表达水平。结果镉可上调PI3K/Akt和ERK1/2的表达;当加入N-乙酰半胱氨酸(NAC)预处理后对镉引起的ERK1/2上调具有抑制作用,但对镉引起的PI3K/Akt上调的抑制作用不明显。结论镉诱导肾细胞凋亡可能与活化PI3K/Akt和ERK1/2通路有关,NAC拮抗镉性肾细胞凋亡的机制可能与抑制镉引起的ERK1/2表达上调有关。
Objective To investigate the effects of cadmium (Cd) on the apoptosis of porcine renal proximal tubule epithelial cells (LLC-PK1) and the expression of intracellular protein kinase B (PI3K / Akt) and extracellular signal-regulated kinase (ERK1 / 2). Methods LLC-PK1 was treated with Cd (0, 10, 20, 40 and 50μmol / L) for different periods of time (0,3,6,12 and 24 h) The expression of intracellular protein kinase B (PI3K / Akt) and extracellular signal - regulated kinase (ERK1 / 2) and their phosphorylated proteins were detected by Western blot. Results Cadmium upregulated the expression of PI3K / Akt and ERK1 / 2. Pretreatment with NAC induced inhibition of ERK1 / 2 upregulation induced by cadmium, but upregulated PI3K / Akt induced by cadmium The inhibitory effect is not obvious. Conclusion Cadmium-induced renal cell apoptosis may be related to the activation of PI3K / Akt and ERK1 / 2 pathways. The mechanism by which NAC antagonizes cadmium-induced renal cell apoptosis may be related to the up-regulation of ERK1 / 2 induced by cadmium.